title: [STAT3 inhibitor].
abstract: Clinical efficacies of various molecular-targeted drugs have been recently demonstrated. Most of these drugs are kinase inhibitors. A most successful drug Glivec is an inhibitor of Bcr-Abl fusion kinase, derived from a well-known causative chromosome translocation of chronic myeloid leukemia(CML). Although other kinase inhibitors have also proved to be useful in the therapy of malignant diseases including an ALK inhibitor for lung carcinomas, a general problem of kinase inhibitors is their lowspecificities. Therefore, the complication of these drugs must be overcome. Recently, trials to develop moleculartargeted therapy whose targets are molecules other than kinases have also been promising. Among molecular targets, STAT3 has attracted a great deal of researchers' attention because it is constitutively activated in most malignant tumors and plays important roles in carcinogenesis. This article summarizes the current situation and problems to be solved with STAT3 inhibitors as well as our recent findings on the molecular mechanisms of STAT3 activation.
authors.affiliation: Division of Cellular Therapy and Division of Stem Cell Signaling, The Institute of Medical Science, The University of Tokyo, Japan.
authors.forename: Toshio
authors.initials: T
authors.lastname: Kitamura
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D006801:Humans; D058990:Molecular Targeted Therapy; D009369:Neoplasms / Q000188:drug therapy* / Q000378:metabolism; D050796:STAT3 Transcription Factor / Q000037:antagonists & inhibitors* / Q000378:metabolism; D054852:Small Molecule Libraries / Q000627:therapeutic use
chemical_list: D000970:Antineoplastic Agents; D050796:STAT3 Transcription Factor; D054852:Small Molecule Libraries